乙肝病毒免疫逃逸突变体及其野生型的包膜蛋白的救援

StephenW

http://jvi.asm.org/content/87/4/2352.abstract?etoc
Impaired Virion Secretion by Hepatitis B Virus Immune Escape Mutants and Its Rescue by Wild-Type Envelope Proteins or a Second-Site Mutation
由乙肝病毒免疫逃逸突变体及其野生型的包膜蛋白的救援或第二位点突变的病毒粒子分泌受损
    Karen Kweia,*,
    Xiaoli Tanga,*,
    Anna S. Lokb,
    Camille Sureauc,
    Tamako Garciaa,*,
    Jisu Lia,
    Jack Wandsa and
    Shuping Tonga

- Author Affiliations

    aLiver Research Center, Rhode Island Hospital, Brown University, Providence, Rhode Island, USA
    bDivision of Gastroenterology and Hepatology, University of Michigan Health Systems, Ann Arbor, Michigan, USA
    cLaboratoire de Virologie Moleculaire, INTS, Paris, France

ABSTRACT

Hepatitis B virus immune escape mutants have been associated with vaccine failure and reinfection of grafted liver despite immune prophylaxis, but their biological properties remain largely unknown. Transfection of 20 such mutants in a human hepatoma cell line identified many with severe impairment in virion secretion, which can be rescued to various extents by coexpression of wild-type envelope proteins or introduction of a novel glycosylation site. Consistent with their role in maintaining intra- or intermolecular disulfide bonds, cysteine residues within the “a” determinant are critical for virion secretion.

StephenW

摘要

尽管免疫预防疫苗的失败和移植肝的再感染B型肝炎病毒的免疫逃避突变相关，但其生物学特性仍是未知。 20个突变体转染的人肝癌细胞系中发现了许多严重的病毒颗粒的分泌，从而可以救出共表达野生型包膜蛋白或引进一种新的糖基化位点不同程度地受到损害。按照它们的作用，在维持内或分子间二硫键的半胱氨酸残基，在“a”决定是病毒颗粒的分泌的关键。